Subpopulations of T-cells which mediate delayed-type hypersensitivity reactions resulting in inflammation of the eye can be differentiated from T-cells which may be cytotoxic for damaged corneal cells because the former subpopulation has the Lyl+ phenotype and their immunological specificities are controlled by Ir gene products of the major histocompatibility gene complex (MHC) while cytotoxic T-cells have the Ly23+ phenotype and their immunological specificities are controlled by D or K gene products of the MHC. The goal of the research in this application is to apply this immunological knowledge to the investigation of inflammation in herpes induced ocular disease by identifying the subpopulations of T-cells involved in mediating inflammation in the eye and to determine if inflammatory reactions mediated by these T-cells are actually needed by the host for resistance to herpes infection. The activities of T-cell subpopulations will be tested by adoptively transferring Lyl+ or Ly23+ HSV-1 sensitized T-cell subpopulations into susceptible mice and then measuring the ability of the transferred cells to protect animals from corneal herpes infection. Control of T-cell specificity by products of the MHC will be studied in order to determine if genes which control delayed-type hypersensitivity reactions govern the generation of immunity to corneal herpes infection or whether T-cell specificity is controlled by genes which govern the generation of cytotoxic T-cells. This information will be obtained by adoptive transfer experiments between congenic mouse strains which differ in Ir regions or K and D regions of the MHC gene complex.